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Is there an evolutionary mismatch between the normal physiology of the human dopaminergic system and current environmental conditions in industrialized countries?

A large body of evidence has recently defined a field theory known as 'evolutionary mismatch', which derives its attributes largely from the fact that current environmental conditions are completely different from those in which the human central nervous system evolved. Current views on the evolutionary mismatch theory lack, however, any attempts to define which brain areas or neuronal circuits should be mostly involved in coding such misevolved traits and to what extent our neurobiological knowledge can be applied to the topographical localization of a specific psychopathology. In this respect the mesocorticolimbic dopaminergic circuits have long been misconceptualized as simple reward or reinforcement systems. Instead, they motivate and coordinate the functions of the higher brain areas that mediate planning and foresight and direct finalized movement in both animals and humans. These systems make animals intensely interested in exploring the world around them, but by the same means they also make them susceptible to the environmental stimuli that have been sought and consumed. It is has been speculated that the cortical dopamine targets that developed most recently in phylogeny are of particular functional value, and that the mesocorticolimbic dopaminergic system is involved in more complex integrative functions than previously assumed. In the present paper I will argue that some mental disorders may have their deep roots in the evolutionary mismatch between the normal physiology of the mesocorticolimbic dopaminergic system and the current environmental conditions in affluent societies.

Animals↗

Developmental changes in brain TRH and in plasma and pituitary TSH and prolactin levels in the rat.

TRH in the hypothalamus and the rest of the brain, as well as TSH and prolactin in the pituitary gland and the plasma have been determined by radioimmunoassay in rats varying in age (10- to 22-day-old fetuses and 1- to 60-day-old rats). TRH is first detected on the 16th day of gestation and its maximum increase occurs during the first 3 weeks of life both in the hypothalamus and the rest of the brain. The evolution patters of TSH and prolactin in the plasma and the pituitary gland are discussed in relation to TRH levels in the brain and in the hypothalamus.

Aging↗

Molecular evolution of the growth hormone-releasing hormone/pituitary adenylate cyclase-activating polypeptide gene family. Functional implication in the regulation of growth hormone secretion.

Growth hormone-releasing hormone (GHRH) and pituitary adenylate cyclase-activating polypeptide (PACAP) belong to the same superfamily of regulatory neuropeptides and have both been characterized on the basis of their hypophysiotropic activities. This review describes the molecular evolution of the GHRH/PACAP gene family from urochordates to mammals and presents the hypothesis that the respective roles of GHRH and PACAP in the control of GH secretion are totally inverted in phylogenetically distant groups of vertebrates. In mammals, GHRH and PACAP originate from distinct precursors whereas, in all submammalian taxa investigated so far, including birds, amphibians and fish, a single precursor encompasses a GHRH-like peptide and PACAP. In mammals, GHRH-containing neurons are confined to the infundibular and dorsomedial nuclei of the hypothalamus while PACAP-producing neurons are widely distributed in hypothalamic and extrahypothalamic areas. In fish, both GHRH- and PACAP-immunoreactive neurons are restricted to the diencephalon and directly innervate the adenohypophysis. In mammals and birds, GHRH plays a predominant role in the control of GH secretion. In amphibians, both GHRH and PACAP are potent stimulators of GH release. In fish, PACAP strongly activates GH release whereas GHRH has little or no effect on GH secretion. The GHRH/PACAP family of peptides thus provides a unique model in which to investigate the structural and functional facets of evolution.

Amino Acid Sequence↗

Birth and adaptive evolution of a hominoid gene that supports high neurotransmitter flux.

The enzyme glutamate dehydrogenase (GDH) is important for recycling the chief excitatory neurotransmitter, glutamate, during neurotransmission. Human GDH exists in housekeeping and brain-specific isotypes encoded by the genes GLUD1 and GLUD2, respectively. Here we show that GLUD2 originated by retroposition from GLUD1 in the hominoid ancestor less than 23 million years ago. The amino acid changes responsible for the unique brain-specific properties of the enzyme derived from GLUD2 occurred during a period of positive selection after the duplication event.

Animals↗

Brain parenchyma apparent diffusion coefficient alterations associated with experimental complex partial status epilepticus.

The objective of this study was to evaluate whether water apparent diffusion coefficient (ADC) measurements provide more specific information than T2-weighted MRI about the evolution of brain parenchyma lesions secondary to prolonged complex partial seizures. We measured the ADC in the brain of rats exhibiting prolonged complex partial seizures induced by intraperitoneal injection of kainic acid (KA). The animals were imaged with diffusion and T2-weighted MRI at 2 T from 3 h up to 9 days after KA injection. In the piriform cortex and amygdala, the T2-weighted MRI signal intensity appeared to be uniformly increased from 24 to 72 h after KA injection, and returned to normal by 9 days. In the same regions between 24 and 72 h, the ADC first decreased and then increased. The ADC changes were consistent with the known histopathologic alterations. In this complex partial seizure model, the ADC measurement provides more specific information than T2-weighted MRI about the histopathologic evolution of the lesions. This supports the proposal that diffusion MRI may be valuable for the evaluation of the neuropathologic sequelae in patients with multiple or prolonged seizures.

Animals↗

Mesotocin and oxytocin in the brain and plasma of an Australian marsupial, the northern brown bandicoot, Isoodon macrourus.

1. Mesotocin (MT) and oxytocin (OT) were measured in the brain and plasma of bandicoots using reverse phase high performance liquid chromatography and specific radioimmunoassays. 2. MT and OT were found in the pituitary (1.25 +/- 0.10 micrograms/MT; 0.725 +/- 0.077 micrograms/OT) and hypothalamus (38.37 +/- 6.46 ng/MT; 19.1 +/- 4.61 ng/OT). Smaller amounts were present in the cerebral cortex. 3. Basal plasma concentrations ranged from 1.5 to 8.1 pg/ml for both peptides (N = 14) and were elevated by stress. 4. It was concluded that both MT and OT are secreted by the bandicoot brain and that stress stimulates secretion.

Animals↗

The origins of cerebral asymmetry: a review of evidence of behavioural and brain lateralization in fishes, reptiles and amphibians.

Early evidence for lateralization at a population and/or individual level in 'lower' vertebrates is reviewed. The lateralities include structural asymmetries in the epithalamus of several species of fish and amphibians, asymmetries in the location of both eyes on the same side of the head and of the dorsal/ventral crossing at optic-chiasma in flatfish, asymmetries in copulatory organs of several species of fishes, asymmetries in lung size and direction of coiling in reptiles, and asymmetrical distribution of scarring in whitefish. More recent data on functional lateralization at population level in lower vertebrates are also reviewed. These include: lateral asymmetries in the direction of turning during escape behaviour and in eye use in poeciliid fish; lateralization of pectoral stridulation sounds in catfish; neural lateralization for control of vocalization in the frogs; pawedness in toads; lateralization of courtship behaviour in newts; and lateralization of aggressive responses in lizards. Several cases of behavioural asymmetries at the individual level are also described, and possible relationships between lateralization at the individual level and fluctuating asymmetries arising from reduced heterozygosity are discussed. It is argued that the overall evidence now available supports the hypothesis of an early origin of brain lateralization in vertebrates.

Amphibians↗

Clinical and pathologic correlates of brain stem auditory response abnormalities.

Short-latency auditory evoked responses were recorded in over 100 neurologic patients. Abnormalities of each response component were correlated with postmortem or radiologic localization of different brain stem lesions. These findings suggested that waves I-VII largely reflect activity at the following levels of the auditory pathway: acoustic nerve (I), pontomedullary junction (II), caudal pons (III), rostral pons or midbrain (IV), midbrain (V), thalamus (VI), and thalamus or auditory radiation (VII). When this information was applied prospectively to the evaluation of brain stem dysfunction, response abnormalities proved useful in detecting and localizing certain lesions not revealed by other tests. Serial recordings provided information about the evolution of brain stem lesions and their response to therapy.

Adult↗

Do we owe our intelligence to a predatory past?

As I am not a neuroscientist, it is an unexpected pleasure for me to contribute a lecture to the James Arthur series on the Evolution of the Human Brain. By contrast, I am an African naturalist, and what I have to say will be very much from the perspective of African cave taphonomy, a recent and rather macabre discipline that uses fossils in an attempt to reconstruct the circumstances of death of the animals involved, as well as to gain insights into their behavior and the paleoecology of the time. The lecture's focus will be on predation, to which I am largely indebted to Professor Raymond Dart, who provoked me into devoting many years of my life developing the principles of cave taphonomy and interpreting the bone accumulations in southern African caves where hominid fossils have been found.

Africa↗

Sequential study of central and peripheral nervous system involvement in an infant with merosin-deficient congenital muscular dystrophy.

Diffuse white matter changes on brain imaging and peripheral neuropathy are associated features of merosin-deficient congenital muscular dystrophy (CMD). In this report we describe the early manifestation and evolution of brain changes, and the involvement of the peripheral nervous system in a female infant with merosin-deficient CMD diagnosed in the neonatal period who had sequential clinical, neurophysiological and magnetic resonance imaging (MRI) assessment. Both MRI and nerve conduction velocity in the first week of life failed to demonstrate any abnormality. By 6 months of age both nerve conduction and MRI were abnormal. White matter changes became more evident on a further scan at 1 yr of age and this pattern remained unchanged on the following scan performed at 17 months of age. Our findings suggest a failure in the physiological maturation process of myelination of both the central and peripheral nervous system.

Central Nervous System Diseases↗